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Curcumin modulation of atherosclerosis and hepatosteatosis in LDLr−/− mice
Author(s) -
Hasan Syeda Tahira,
Zingg JeanMarc,
Noble Timothy,
Kwan Paul,
Smith Donald,
Meydani Mohsen
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.359.1
Subject(s) - curcumin , endocrinology , medicine , inflammation , ldl receptor , obesity , chemistry , pharmacology , cholesterol , lipoprotein
Limited animal studies reported that curcumin (Cur), a bioactive component of turmeric spice, suppresses atherosclerosis, an inflammatory disease of arteries, but the mechanism for these effects is largely unknown. LDLr−/ − mice were fed high fat (HF) diet supplemented with increasing Cur doses (500, 1,000, 1,500 mg/kg diet) for 16 wks. Cur reduced BW and fat gain although fecal fat excretion was less than control's suggesting increased catabolism. Medium dose Cur diet (1,000 mg/kg) significantly reduced aortic fatty streaks and suppressed IL‐6 and MCP‐1 expression in aortas, but high dose diet (1,500 mg/kg) had adverse effect on these parameters and increased plasma levels of several inflammatory cytokines including IL‐6, IL‐10, IL‐12. This U‐shaped trend was also present when aortic roots were examined for fatty lesions, fibrotic deposits, FABP‐4/aP2 and VCAM‐1 expression. Of note, Cur at high dose suppressed hepatosteatosis, reduced fibrotic tissue, and preserved liver glycogen levels. While complex mechanisms are involved in Cur suppression of HF diet‐induced atherosclerosis and obesity, Cur suppression of aP2 and VCAM‐1 expression in aortic root lesions and aP2 expression in macrophages along with reduction of inflammatory cytokines provide an insight to the potential mechanism by which Cur suppresses atherogenesis and obesity. NIFA/USDA grant #2010–65200‐20395 &USDA contract #58–1950‐0–014.